Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) were defined by a panel of experts in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) as the Berlin Definition. Presently there are three stages: mild, moderate, and severe with an associated increased mortality and increased median duration of mechanical ventilation in survivors. As shown by the Berlin Definition of Acute Respiratory Distress Syndrome (Table VII), the categories of ARDS are based in part on the degree of hypoxemia determined by the ratio of PaO2/FiO2, where the PaO2 is the partial pressure of oxygen in arterial blood and the FiO2 is the fraction of inspired oxygen. Management of ARDS includes treatment of the underlying condition, mechanical or noninvasive ventilation, fluid and hemodynamic therapy, treatment of opportunistic infection, nutrition, and pharmacologic therapy. Currently there is no specific pharmacologic therapy for ALI/ARDS. Agents that have failed in large trials include in part, glucocorticoids, alprostadil, surfactant, ketoconazole, N-acetylcysteine, procysteine, lisofylline, and site-inactivated recombinant factor VIIa. Given the concern for the increased risk of nosocomial infection or critical illness polyneuropathy, as well as the lack of improvement in mortality, the routine use of glucocorticoids in ARDS is not recommended.
Hypoxic-ischemic brain injury is a general classification of brain injury which includes, in part, brain trauma, cardiac arrest, vascular catastrophe (hemorrhagic, thrombotic stroke), poisoning (such as carbon monoxide or drug overdose) and central nervous system infection. Improved techniques have resulted in greater numbers of patients surviving with variable degrees of brain injury. The evolution of hypothermic treatment has been particularly useful in improving neurologic morbidity and decreasing mortality in survivors of cardiac arrest and major brain trauma. The induction of mild to moderate hypothermia to a target temperature of 32-34° C. has improved the neurologic outcomes; however, refinement of existing protocols with validated studies are needed.
Supportive and preventive care measures remain the mainstay of therapy in all forms of hypoxic-ischemic brain injury. In additions to concerted efforts to restore the central nervous system to its pre jury state, clinicians are additionally focused on preventing nosocomial infection, providing adequate nutrition and providing adequate prophylaxis against venous thromboembolism, and gastric stress ulceration.
Severe traumatic brain injury is defined as head trauma associated with a GlasgowComa Scale (GCS) score of 3-8. Traditionally, steroids were used in high doses for the treatment of traumatic brain injury to decrease the swelling and edema cause by the primary injury (such as skull fracture, cerebral contusion, and hemorrhage). However, more recently, a consensus of opinion holds that high-dose steroids increase the risk of secondary infection, gastric ulceration, electrolyte imbalance, fluid retention, and steroid induced diabetes mellitus. Moreover, high-dose methylprednisolone in the treatment of patients with severe traumatic brain injury was recently considered a contraindication.